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Print version ISSN 0034-7094

Rev. Bras. Anestesiol. vol.57 no.4 Campinas July/Aug. 2007

http://dx.doi.org/10.1590/S0034-70942007000400015

LETTER
TO THE EDITOR

Is it possible
to use hydrocortisone to treat post-spinal anesthesia headache?

To the Editor,

Postural postdural puncture headache (PPDPH) is a known
complication, but rare nowadays due to the reduced caliber of the
needles compared to the ones used in the past 1. The
current incidence of this type of headache is approximately 2.4%
with a 25G Whitacre needle and 0.4% with the 27G needle of the
same brand 2. The incidence of PPDPH increases when
the same needle is reprocessed 2.

The physiopathology of this painful syndrome is not completely
elucidated 1, but the most accepted cause does not
differ much from that postulated by Bier, based on the loss of
cerebrospinal fluid (CF). The fall in the pressure of the CF with
contraction of painful structures when the patient is erect seems
to be the main reason for the headache 1,3,4. The
normal pressure of the spinal fluid in the horizontal position is
between 5 an 15 cm H2O 1,3, but after dural
puncture, it might fall below 4 cm H2O 3.
Reflex vasodilation in an attempt to correct the reduced
intracranial pressure also contributes for the development of
this symptom 1,3.

The incidence of PPDPH decreases with age and with the use of
small caliber needles 1,3,4. When the studies consider
age differences, the incidence does not seem to be different
between genders 4. The introduction of the needle with
the bevel parallel to the longitudinal axis of the meninges
reduces the incidence of headache, although it is known that
collagen fibers in the dura mater are randomly distributed
1,3,4.

The treatment should be individualized, dependent on the
severity of pain, and it can be clinical or using the epidural
blood patch. Clinical treatment includes bed rest to relieve the
symptoms, intravenous hydration 4-7, and the use of a
few drugs, such as: caffeine 1,3,4,6,7, sumatriptan
1,3, tiapride 3,6, and non-steroidal
anti-inflammatory drugs 1,3,4,6,7.

It has been postulated that PPDPH could affect a specific
group of patients that would be more prone to physiological
stress, and develop accentuated hypercostisolism, with a
different response to trauma and other types of stress
8,9. The increase in cortisol has a negative effect in
the secretion of the adrenocorticotrophic (ACTH) hormone and
counteracts its beneficial effects 9.

ACTH has been used in cases of failure of the blood patch and
in patients refractory to conservative measures 3,7.
It has a 70% 7-10 efficacy rate and can be
administered IV or IM 8. After administration, the
peak concentration is reached in 6 to 8 hours 11.

The mechanisms of action proposed for ACTH include: increased
production of spinal fluid and beta-endorphins 9,10,12
and release of steroids by the adrenal glands 9,11,12.
ACTH and beta-endorphins originate from the same precursor
molecule, a proopiomelanocortin, and when ACTH is cleaved
enzymatically, it generates metabolites that are used in the
production of beta-endorphins 9. The anti-inflammatory
effects of ACTH could be secondary to the release of cortisol and
corticosterone by the adrenal glands 9.

Considering that the actions of ACTH could be through the
release of endogenous glucocorticoids and the fact that this drug
is not readily obtainable in some countries, researchers started
to report the use of hydrocortisone in place of ACTH in the
treatment of PPDPH with success 6,7,12,13.
Hydrocortisone has an anti-inflammatory action, and it can act at
the level of the Na/K ATPase pump, increasing the production of
CF. On the other hand, one should remember that the painful
syndrome may resolve spontaneously and independent of the use or
not of hydrocortisone, and that this indicates it should be used
carefully and even leads one to question its analgesic efficacy.
Further studies with better methodological quality are needed to
define the true role of this drug in the treatment of PPDPH, as
well as the ideal dose.